Low-energy diets differing in fibre, red meat and coffee intake equally improve insulin sensitivity in type 2 diabetes: a randomised feasibility trial

Aims/hypothesis Epidemiological studies have found that a diet high in fibre and coffee, but low in red meat, reduces the risk for type 2 diabetes. We tested the hypothesis that these nutritional modifications differentially improve whole-body insulin sensitivity (primary outcome) and secretion. Met...
Ausführliche Beschreibung

Aims/hypothesis Epidemiological studies have found that a diet high in fibre and coffee, but low in red meat, reduces the risk for type 2 diabetes. We tested the hypothesis that these nutritional modifications differentially improve whole-body insulin sensitivity (primary outcome) and secretion. Methods Inclusion criteria were: age 18–69 years, BMI ≥30 kg/$ m^{2} $, type 2 diabetes treated with diet, metformin or acarbose and known disease duration of ≤5 years. Exclusion criteria were: $ HbA_{1c} $ >75 mmol/mol (9.0%), type 1 or secondary diabetes types and acute or chronic diseases including cancer. Patients taking any medication affecting the immune system or insulin sensitivity, other than metformin, were also excluded. Of 59 patients (randomised using randomisation blocks [four or six patients] with consecutive numbers), 37 (54% female) obese type 2 diabetic patients completed this controlled parallel-group 8-week low-energy dietary intervention. The participants consumed either a diet high in cereal fibre (whole grain wheat/rye: 30–50 g/day) and coffee (≥5 cups/day), and free of red meat (L-RISK, n = 17) or a diet low in fibre (≤10 g/day), coffee-free and high in red meat (≥150 g/day) diet (H-RISK, n = 20). Insulin sensitivity and secretion were assessed by hyperinsulinaemic–euglycaemic clamp and intravenous glucose tolerance tests with isotope dilution. Whole-body and organ fat contents were measured by magnetic resonance imaging and spectroscopy. Results Whole-body insulin sensitivity increased in both groups (mean [95% CI]) (H-RISK vs L-RISK: 0.8 [0.2, 1.4] vs 1.0 [0.4, 1.7] mg $ kg^{−1} $ $ min^{−1} $, p = 0.59), while body weight decreased (−4.8% [−6.1%, −3.5%] vs −4.6% [−6.0%, −3.3%], respectively). Hepatic insulin sensitivity remained unchanged, whereas hepatocellular lipid content fell in both groups (−7.0% [−9.6%, −4.5%] vs −6.7% [−9.5%, −3.9%]). Subcutaneous fat mass (−1,553 [−2,767, −340] $ cm^{3} $ vs −751 [−2,047; 546] $ cm^{3} $, respectively) visceral fat mass (−206 [−783, 371] $ cm^{3} $ vs −241 [−856, 373] $ cm^{3} $, respectively) and muscle fat content (−0.09% [−0.16%, −0.02%] vs −0.02% [−0.10%, 0.05%], respectively) decreased similarly. Insulin secretion remained unchanged, while the proinflammatory marker IL-18 decreased only after the L-RISK diet. Conclusions/interpretation No evidence of a difference between both low-energy diets was identified. Thus, energy restriction per se seems to be key for improving insulin action in phases of active weight loss in obese type 2 diabetic patients, with a potential improvement of subclinical inflammation with the L-RISK diet. Trial Registration: Clinicaltrials.gov NCT01409330 Funding: This study was supported by the Ministry of Science and Research of the State of North Rhine-Westphalia (MIWF NRW), the German Federal Ministry of Health (BMG), the Federal Ministry for Research (BMBF) to the Center for Diabetes Research (DZD e.V.) and the Helmholtz Alliance Imaging and Curing Environmental Metabolic Diseases (ICEMED). Ausführliche Beschreibung

Autor*in:	Nowotny, Bettina [verfasserIn] Zahiragic, Lejla Bierwagen, Alessandra Kabisch, Stefan Groener, Jan B. Nowotny, Peter J. Fleitmann, Ann Kristin Herder, Christian Pacini, Giovanni Erlund, Iris Landberg, Rikard Haering, Hans-Ulrich Pfeiffer, Andreas F. H. Nawroth, Peter P. Roden, Michael

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Diet Inflammation Insulin sensitivity Type 2 diabetes Weight loss

Anmerkung:	© Springer-Verlag Berlin Heidelberg 2014

Übergeordnetes Werk:	Enthalten in: Diabetologia - Berlin : Springer, 1965, 58(2014), 2 vom: 26. Nov., Seite 255-264
Übergeordnetes Werk:	volume:58 ; year:2014 ; number:2 ; day:26 ; month:11 ; pages:255-264

Links:	Volltext

DOI / URN:	10.1007/s00125-014-3457-8

Katalog-ID:	SPR001001914